ArticleMolecular and cellular biology2002
Characterization of a high-molecular-weight Notch complex in the nucleus of Notch(ic)-transformed RKE cells and in a human T-cell leukemia cell line.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 143 citations in OpenAlex.
- HP1γ promotes the progression of colorectal cancer through interaction with RBPJ of the Notch signaling pathway.Cell biology and toxicology · 2026Article
- A novel chemical attack on Notch-mediated transcription by targeting the NACK ATPase.Molecular therapy oncolytics · 2023Article
- NACK and INTEGRATOR act coordinately to activate Notch-mediated transcription in tumorigenesis.Cell communication and signaling : CCS · 2021Article
- Pharmacological Disruption of the Notch1 Transcriptional Complex Inhibits Tumor Growth by Selectively Targeting Cancer Stem Cells.Cancer research · 2021Article
- Positive autoregulation ofDevelopment (Cambridge, England) · 2020Article
- Role of MAML1 in targeted therapy against the esophageal cancer stem cells.Journal of translational medicine · 2019Article
- Inhibition of Mastermind-like 1 alleviates liver fibrosis induced by carbon tetrachloride in rats.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- Role of MAML1 and MEIS1 in Esophageal Squamous Cell Carcinoma Depth of Invasion.Pathology oncology research : POR · 2018Article
- Notch Represses Transcription by PRC2 Recruitment to the Ternary Complex.Molecular cancer research : MCR · 2017Article
- Fucosylation Deficiency in Mice Leads to Colitis and Adenocarcinoma.Gastroenterology · 2017Article
- The Small Molecule IMR-1 Inhibits the Notch Transcriptional Activation Complex to Suppress Tumorigenesis.Cancer research · 2016Article
- Aberrant Notch Signaling in the Bone Marrow Microenvironment of Acute Lymphoid Leukemia Suppresses Osteoblast-Mediated Support of Hematopoietic Niche Function.Cancer research · 2016Article
- Notch Signaling in Neuroendocrine Tumors.Frontiers in oncology · 2016Review
- Repression of Ccr9 transcription in mouse T lymphocyte progenitors by the Notch signaling pathway.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Colocalization of β-catenin with Notch intracellular domain in colon cancer: a possible role of Notch1 signaling in activation of CyclinD1-mediated cell proliferation.Molecular and cellular biochemistry · 2014Article
- NACK is an integral component of the Notch transcriptional activation complex and is critical for development and tumorigenesis.Cancer research · 2014Article
- Wnt-Notch signalling crosstalk in development and disease.Cellular and molecular life sciences : CMLS · 2014Review
- Inhibition of CK2α down-regulates Notch1 signalling in lung cancer cells.Journal of cellular and molecular medicine · 2013Article
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- VEGF and Notch in tip and stalk cell selection.Cold Spring Harbor perspectives in medicine · 2013Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Notch genes encode a family of transmembrane proteins that are involved in many cellular processes, such as differentiation, proliferation, and apoptosis. It is well established that all four Notch genes can act as oncogenes; however, the mechanism by which Notch proteins transform cells remains unknown. Previously, we reported that both nuclear localization and transcriptional activation are required for neoplastic transformation of RKE cells. Furthermore, we identified cyclin D1 as a direct transcriptional target of constitutively active Notch molecules. In an effort to understand the mechanism by which Notch functions in the nucleus, we sought to determine if Notch formed stable complexes using size exclusion chromatography. Herein, we report that the Notch intracellular domain (N(ic)) forms distinct high-molecular-weight complexes in the nuclei of transformed RKE cells. The largest complex is approximately 1.5 MDa and contains both endogenous CSL (for CBF1, Suppressor of Hairless, and Lag-1) and Mastermind-Like-1 (Maml). N(ic) molecules that do not have the high-affinity binding site for CSL (RAM) retain the ability to associate with CSL in a stable complex through interactions involving Maml. However, Maml does not directly bind to CSL. Furthermore, Maml can rescue Delta RAM transcriptional activity on a CSL-dependent promoter. These results indicate that deletion of the RAM domain does not equate to CSL-independent signaling. Moreover, in SUP-T1 cells, N(ic) exists exclusively in the largest N(ic)-containing complex. SUP-T1 cells are derived from a T-cell leukemia that harbors the t(7;9)(q34;q34.3) translocation and constitutively express N(ic). Taken together, our data indicate that complex formation is likely required for neoplastic transformation by Notch(ic).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.